| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Rui Song, Jie Zhang, Lijuan Zhang, Guanghua Wang, Da Wo, Jian Feng, Xucheng Li, Jue L. H2O 2 induces myocardial hypertrophy in H9c2 cells: a potential role of Ube3a. Cardiovascular toxicology. vol 15. issue 1. 2015-11-12. PMID:24917194. |
our results showed that 10-20 μm h2o2 can induce myocardial hypertrophy without affecting cell viability and inducing cell apoptosis, while the corresponding transcription and translation levels of ube3a are significantly increased during the process. |
2015-11-12 |
2023-08-13 |
rat |
| Bei Liu, Zhiye Wu, Yunpeng Li, Caiwen Ou, Zhenjun Huang, Jianwu Zhang, Peng Liu, Chengfeng Luo, Minsheng Che. Puerarin prevents cardiac hypertrophy induced by pressure overload through activation of autophagy. Biochemical and biophysical research communications. vol 464. issue 3. 2015-11-10. PMID:26188094. |
administration of puerarin for 6 weeks effectively restricted cardiomyocyte hypertrophy and apoptosis. |
2015-11-10 |
2023-08-13 |
rat |
| Bei Liu, Zhiye Wu, Yunpeng Li, Caiwen Ou, Zhenjun Huang, Jianwu Zhang, Peng Liu, Chengfeng Luo, Minsheng Che. Puerarin prevents cardiac hypertrophy induced by pressure overload through activation of autophagy. Biochemical and biophysical research communications. vol 464. issue 3. 2015-11-10. PMID:26188094. |
all these data indicate that puerarin exerts protective effects against cardiomyocyte hypertrophy and apoptosis, partly by restoration of autophagy through ampk/mtor-mediated signaling. |
2015-11-10 |
2023-08-13 |
rat |
| Merih Önal, Taner Yılmaz, Elif Bilgiç, Sevda Fatma Müftüoğlu, Oğuz Kuşçu, Rıza Önder Günaydı. Apoptosis in chronic tonsillitis and tonsillar hypertrophy. International journal of pediatric otorhinolaryngology. vol 79. issue 2. 2015-10-28. PMID:25555639. |
apoptosis in chronic tonsillitis and tonsillar hypertrophy. |
2015-10-28 |
2023-08-13 |
Not clear |
| Juan-Juan Sheng, Hui Chang, Zhi-Bin Y. Nuclear Translocation of Calpain-2 Mediates Apoptosis of Hypertrophied Cardiomyocytes in Transverse Aortic Constriction Rat. Journal of cellular physiology. vol 230. issue 11. 2015-10-13. PMID:25820375. |
apoptosis of cardiomyocytes plays an important role in the transition from cardiac hypertrophy to heart failure. |
2015-10-13 |
2023-08-13 |
rat |
| Asmund T Roe, Michael Frisk, William E Louc. Targeting cardiomyocyte Ca2+ homeostasis in heart failure. Current pharmaceutical design. vol 21. issue 4. 2015-09-25. PMID:25483944. |
disrupted cardiomyocyte ca(2+) homeostasis is recognized as a major contributor to the heart failure phenotype, as it plays a key role in systolic and diastolic dysfunction, arrhythmogenesis, and hypertrophy and apoptosis signaling. |
2015-09-25 |
2023-08-13 |
Not clear |
| Chunlai Zeng, Peng Zhong, Yunjie Zhao, Karvannan Kanchana, Yali Zhang, Zia A Khan, Subrata Chakrabarti, Lianpin Wu, Jingying Wang, Guang Lian. Curcumin protects hearts from FFA-induced injury by activating Nrf2 and inactivating NF-κB both in vitro and in vivo. Journal of molecular and cellular cardiology. vol 79. 2015-09-17. PMID:25444713. |
we observed that palmitate (pa) treatment in cardiac derived h9c2 cells induced a marked increase in reactive oxygen species, inflammation, apoptosis and hypertrophy. |
2015-09-17 |
2023-08-13 |
mouse |
| Chunlai Zeng, Peng Zhong, Yunjie Zhao, Karvannan Kanchana, Yali Zhang, Zia A Khan, Subrata Chakrabarti, Lianpin Wu, Jingying Wang, Guang Lian. Curcumin protects hearts from FFA-induced injury by activating Nrf2 and inactivating NF-κB both in vitro and in vivo. Journal of molecular and cellular cardiology. vol 79. 2015-09-17. PMID:25444713. |
in addition, oral administration of curcumin at 50mg/kg completely suppressed high fat diet-induced oxidative stress, inflammation, apoptosis, fibrosis, hypertrophy and tissue remodeling in mice. |
2015-09-17 |
2023-08-13 |
mouse |
| Michael G Katz, Anthony S Fargnoli, Richard D Williams, Andrew P Kendle, Nury M Steuerwald, Charles R Bridge. MiRNAs as potential molecular targets in heart failure. Future cardiology. vol 10. issue 6. 2015-09-04. PMID:25495820. |
genetic data have identified the roles of mirnas in basic pathological processes associated with heart failure: apoptosis, fibrosis, myocardial hypertrophy and cardiac remodeling. |
2015-09-04 |
2023-08-13 |
Not clear |
| Bodong Lv, Jianfeng Zhao, Fan Yang, Xiaojun Huang, Gang Chen, Kebing Yang, Shanshan Liu, Chunlei Fan, Huiying Fu, Zhaodian Che. Phenotypic transition of corpus cavernosum smooth muscle cells subjected to hypoxia. Cell and tissue research. vol 357. issue 3. 2015-09-01. PMID:24913687. |
our results showed that ccsmcs became hypertrophic with loss of myofilament bundles and formation of an extensive rough endoplasmic reticulum (rer) under hypoxic conditions, with inhibited cell proliferation and enhanced cell apoptosis. |
2015-09-01 |
2023-08-13 |
Not clear |
| Peng Zhong, Lianpin Wu, Yuanyuan Qian, Qilu Fang, Dandan Liang, Jingying Wang, Chunlai Zeng, Yi Wang, Guang Lian. Blockage of ROS and NF-κB-mediated inflammation by a new chalcone L6H9 protects cardiomyocytes from hyperglycemia-induced injuries. Biochimica et biophysica acta. vol 1852. issue 7. 2015-08-27. PMID:25736300. |
pretreatment with l6h9 significantly reduced high glucose-induced inflammatory cytokine expression, ros level increase, mitochondrial dysfunction, cell apoptosis, fibrosis, and hypertrophy in h9c2 cells, which may be mediated by nf-κb inhibition and nrf2 activation. |
2015-08-27 |
2023-08-13 |
mouse |
| Peng Zhong, Lianpin Wu, Yuanyuan Qian, Qilu Fang, Dandan Liang, Jingying Wang, Chunlai Zeng, Yi Wang, Guang Lian. Blockage of ROS and NF-κB-mediated inflammation by a new chalcone L6H9 protects cardiomyocytes from hyperglycemia-induced injuries. Biochimica et biophysica acta. vol 1852. issue 7. 2015-08-27. PMID:25736300. |
in mice with stz-induced diabetes, oral administration of l6h9 at 20 mg/kg/day for 8 weeks significantly decreased the cardiac cytokine and ros level, accompanied by decreasing cardiac apoptosis and hypertrophy, and, finally, improved histological abnormalities and fibrosis, without affecting the hyperglycemia. |
2015-08-27 |
2023-08-13 |
mouse |
| Ming-Wei Bao, Xiao-Jing Zhang, Liangpeng Li, Zhongxiang Cai, Xiaoxiong Liu, Nian Wan, Gangying Hu, Fengwei Wan, Rui Zhang, Xueyong Zhu, Hao Xia, Hongliang L. Cardioprotective role of growth/differentiation factor 1 in post-infarction left ventricular remodelling and dysfunction. The Journal of pathology. vol 236. issue 3. 2015-08-25. PMID:25726944. |
compared with control animals, cardiomyocyte apoptosis, inflammation, hypertrophy, and interstitial fibrosis were all remarkably reduced in the gdf1-tg mice following mi. |
2015-08-25 |
2023-08-13 |
mouse |
| Erik Holm, Jane E Aubin, Graeme K Hunter, Frank Beier, Harvey A Goldber. Loss of bone sialoprotein leads to impaired endochondral bone development and mineralization. Bone. vol 71. 2015-08-21. PMID:25464126. |
decreased numbers of tunel-positive hypertrophic chondrocytes were also apparent in the bsp(-/-) tibial growth plates, suggesting decreased apoptosis. |
2015-08-21 |
2023-08-13 |
mouse |
| W Nadru. Myocardial remodeling in hypertension. Journal of human hypertension. vol 29. issue 1. 2015-08-06. PMID:24804791. |
furthermore, the hypertrophic myocardium shows fibrosis, alterations in the coronary circulation and cardiomyocyte apoptosis, which may result in heart failure, myocardial ischemia and arrhythmias. |
2015-08-06 |
2023-08-13 |
human |
| Iman A Mohamed, Fatima Mraich. Targeting osteopontin, the silent partner of Na+/H+ exchanger isoform 1 in cardiac remodeling. Journal of cellular physiology. vol 230. issue 9. 2015-08-04. PMID:25677682. |
cardiac hypertrophy (ch), characterized by the enlargement of cardiomyocytes, fibrosis and apoptosis, contributes to cardiac remodeling, which if left unresolved results in heart failure. |
2015-08-04 |
2023-08-13 |
Not clear |
| Alicia Mattiazzi, Rosana A Bassani, Ariel L Escobar, Julieta Palomeque, Carlos A Valverde, Martín Vila Petroff, Donald M Ber. Chasing cardiac physiology and pathology down the CaMKII cascade. American journal of physiology. Heart and circulatory physiology. vol 308. issue 10. 2015-07-28. PMID:25747749. |
dysregulation of these pathways constitutes a central mechanism of various cardiac disease phenomena, like apoptosis and necrosis during ischemia/reperfusion injury, digitalis exposure, post-acidosis and heart failure arrhythmias, or cardiac hypertrophy. |
2015-07-28 |
2023-08-13 |
Not clear |
| Nora Klöting, Matthias Blühe. Adipocyte dysfunction, inflammation and metabolic syndrome. Reviews in endocrine & metabolic disorders. vol 15. issue 4. 2015-07-23. PMID:25344447. |
importantly, an inability to increase at mass by adipocyte hyperplasia may lead to adipocyte hypertrophy and could induce dysfunction of adipose tissue characterized by decreased insulin sensitivity, hypoxia, increased parameters of intracellular stress, increased autophagy and apoptosis and tissue inflammation. |
2015-07-23 |
2023-08-13 |
Not clear |
| Juan-Juan Sheng, Yan Chen, Hui Chang, Yun-Ying Wang, Bo Jiao, Zhi-Bin Y. Multisite phosphorylation of Bcl-2 via protein kinase Cδ facilitates apoptosis of hypertrophic cardiomyocytes. Clinical and experimental pharmacology & physiology. vol 41. issue 11. 2015-07-20. PMID:25132161. |
multisite phosphorylation of bcl-2 via protein kinase cδ facilitates apoptosis of hypertrophic cardiomyocytes. |
2015-07-20 |
2023-08-13 |
rat |
| Juan-Juan Sheng, Yan Chen, Hui Chang, Yun-Ying Wang, Bo Jiao, Zhi-Bin Y. Multisite phosphorylation of Bcl-2 via protein kinase Cδ facilitates apoptosis of hypertrophic cardiomyocytes. Clinical and experimental pharmacology & physiology. vol 41. issue 11. 2015-07-20. PMID:25132161. |
the aim of the present study was to investigate whether mitochondrial translocation of pkcδ phosphorylates multiple sites of bcl-2, resulting in an imbalance between bcl-2 and bak or bax, thus enhancing the susceptibility of hypertrophic cardiomyocytes to angiotensin ii (angii)-induced apoptosis. |
2015-07-20 |
2023-08-13 |
rat |